Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study investigated the stimulus to pituitary-adrenocortical activity (PACA) during halothane anaesthesia. Groups of six sheep were anaesthetized with thiopentone/halothane (TH group), acepromazine/thiopentone/halothane (ATH group) or pentobarbitone (P group). Dobutamine was infused in the TH and ATH groups to prevent hypotension (0.3-1.4 micrograms/kg/min) and in the P group at 0.05 microgram/kg/min. Pulse rate, arterial blood gases and pressure (ABP) were measured and sequential blood samples taken for assay of cortisol, adrenocorticotrophic hormone (ACTH), arginine vasopressin (AVP), glucose and lactate. Pulse rate increased in all groups. Arterial blood pressure decreased by 13% in TH, by 24% in ATH and remained stable in P. All three groups developed hypercapnia and acidosis but were well oxygenated. Cortisol increased in all groups; with ATH the sevenfold rise occurred earlier than with either TH (sixfold rise) or P (fivefold rise). Adrenocorticotrophic hormone changes were as for cortisol but AVP increases were not consistent. Glucose and lactate were stable, but lactate was lowest with ATH. Dobutamine infusion failed to prevent hypotension during halothane anaesthesia and PACA appeared proportional to the hypotension. Dobutamine may have stimulated ACTH and cortisol release after 120 min. Halothane-induced hypotension may cause adrenocortical activity but a direct effect of halothane cannot be ruled out.
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PMID:Endocrine and metabolic responses in sheep during halothane and pentobarbitone anaesthesia with dobutamine infusion. 950 59

In conscious dogs, arginine vasopressin (AVP) inhibits an angiotensin II drive to ventilation during air breathing and during acute hypercapnia. To determine whether AVP inhibits respiration in rats, as in dogs, respiration and metabolism were measured in six male Sprague-Dawley rats using a plethysmograph. Rats breathed air, followed by 5% and 6.5% CO2 with or without AVP V1 receptor block. In unblocked experiments, minute ventilation (V) increased to a comparable level during inhalation of both CO2 gas mixtures, resulting in a flattening of the ventilatory response to increased Paco2. However, oxygen consumption decreased during 6.5% CO2, compared with 5% CO2, so that the ventilatory equivalent for O2 increased in a more linear manner with respect to Paco2. The main effect of AVP V1 receptor block was to increase mean arterial blood pressure; there was no significant effect of AVP V1 receptor block on respiratory responses. AVP does not inhibit respiration in conscious rats as it does in conscious dogs.
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PMID:Ventilatory and metabolic effects of hypercapnia in conscious rats: AVP V1 receptor block. 979 43

Following exposure of anesthetized and unanesthetized rats to hypercapnic stress, arginine vasopressin (AVP)-containing neurons of the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei were examined for expression of the c-fos gene encoded protein (c-Fos). In addition, we determined whether AVP-containing PVN neurons activated by hypercapnia project to phrenic nuclei. In adult control rats, only scant c-Fos-like immunoreactive neurons were observed within the hypothalamic nuclei. A marked increase in c-Fos positive cells was induced after 2 h of breathing a gas mixture with elevated CO(2) (5% CO(2), 21% O(2) and 74% N(2), or 1 h following breathing of 12% CO(2,) 21% O(2,) and 67% N(2)). Colocalization studies of AVP and c-Fos protein revealed that in the PVN, 75% of AVP-containing cells expressed c-Fos immunoreactivity. c-Fos and AVP were coexpressed in 60% of SON neurons in anesthetized rats. In addition, retrograde labeling studies with cholera toxin b subunit (CTb) revealed that a subpopulation of PVN cells (15%) that project to phrenic nuclei are activated by hypercapnia, as indicated by c-Fos expression. These results indicate that (i) PVN and SON AVP-containing neurons are part of the neuronal networks that react to hypercapnic exposure; and (ii) a subset of CO(2) reactive PVN cells innervate phrenic nuclei.
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PMID:CO(2)-induced c-Fos expression in hypothalamic vasopressin containing neurons. 1178 32

The purpose of the current study was to examine where arginine vasopressin (AVP) inhibits respiration by direct action on the areas of the ventrolateral medulla (VLM) in the rat. The animal was anesthetized by urethane (1.2 g/kg, i.p.), paralyzed with gallamine triethiodide, and artificially ventilated. Catheterization of the femoral artery and vein, and bilateral vagotomy were performed. The rat was then placed upon a stereotaxic instrument in a prone position. The phrenic nerve was separated and cut peripherally. Phrenic nerve activity (PNA) was monitored at normocapnia and hypercapnia in hyperoxia. Microinjection of AVP into various subregions of the VLM was then performed. In response to AVP microinjection, a transient period of apnea and then a significant decrease in PNA amplitude were observed. Arterial blood pressure was unchanged. This inhibition of PNA with AVP treatment was site-specific, attenuated by raising CO2 concentration, and totally abolished by pretreatment with AVP V1A receptor antagonist. Data of the present study indicate that endogenous resource of AVP may produce an inhibitory effect upon respiration via AVP receptors presented on neurons within the VLM.
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PMID:Arginine vasopressin produces inhibition upon respiration without pressor effect in the rat. 1297 98

Chronic obstructive pulmonary disease (COPD) often leads to massive oedema and the development of what is usually called cor pulmonale. The mechanisms by which patients with COPD retain salt and water are not completely understood. Several abnormalities have been found including reduced renal blood flow with relatively preserved glomerular filtration rate and elevated levels of renin, aldosterone, arginine vasopressin and atrial natriuretic peptide. Generally, these abnormalities worsen with the severity of COPD and are most marked during the oedematous phases. Cardiac output is remarkably normal, suggesting that "cor pulmonale" is not primarily a cardiac disorder but rather a condition of volume overload due to activation of sodium-retaining mechanisms. The stimulus for this activation could be underfilling of the arterial system (reduced effective circulating volume) secondary to a fall in total peripheral vascular resistance. The latter is caused by hypercapnia-induced dilation of the precapillary sphincters. Apparently, the massive sodium retention by the kidney is not able to restore the circulating volume and a vicious cycle ensues ultimately leading to a clinical picture which resembles right-sided heart failure. Predictably, only blockade of the effects of carbon dioxide at the level of the precapillary sphincters would be able to halt this process.
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PMID:Fluid homeostasis in chronic obstructive lung disease. 1462 Nov 5

The aim of the study was to examine whether or not arginine vasopressin (AVP) might modulate cardiopulmonary functions by acting on the lateral area of the ventrolateral medulla (VLM) in the rat. The rat was anesthetized, bilaterally vagotomized, paralyzed, ventilated, and then placed on a stereotaxic instrument in a prone position. Activity of the phrenic nerve (PNA) was monitored at normocapnia and hypercapnia in hyperoxia. Microinjection of AVP into the lateral region of the VLM resulted in a brief apnea followed by a significant decrease in PNA amplitude and a concomitant significant increase in blood pressure. The inhibition of PNA with AVP treatment could be partly attenuated by hypercapnia but not by phentolamine. Both inhibition of PNA and pressor response with AVP microinjection into the lateral VLM were totally abolished after pretreatment with AVP V1A receptor antagonist. These results suggest that a vasopressinergic pathway projects to the lateral VLM and modulates cardiopulmonary functions via AVP V1A receptors on neurons within the lateral VLM.
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PMID:Cardiopulmonary response to vasopressin-induced activation on V1A receptors in the lateral ventrolateral medulla in the rat. 1523 92

The area postrema (AP) is the most caudal circumventricular organ in the central nervous system and contains arginine vasopressin (AVP) receptors. To investigate that AVP receptors in the AP might participate in the modulation of respiration, the adult rat was anesthetized with urethane (1.2 g/kg, i.p.), paralyzed, ventilated artificially, and maintained at normocapnia in hyperoxia. The phrenic nerve was separated at C4 level. Phrenic burst was amplified, filtered, integrated, and then stored in the hard disc via the PowerLab system. Three doses of AVP and an AVP V(1A) receptor antagonist, [beta-mercapto-beta,beta-cyclopentamethylenepropionyl1,-O-Me-Tyr2,Arg8]-vasopressin, were microinjected into the AP through a pair of microelectrodes. The moderate and high doses of AVP reduced the PNA to 72% and 45% of the control (P < 0.05), extended the mean TE from 1.4 s before AVP to 4.0 s and 7.6 s, (P < 0.05), and decrease in BP by 26 and 37 mmHg (P < 0.05), respectively. These significant reductions in PNA and BP and elongation of TE were totally abolished by the pre-treatment of the AVP V(1A) receptor antagonist and by application of lidocaine or CoCl2 at the nucleus tractus solitarius (NTS). Moreover, pulmonary inhibition caused by AVP was significantly attenuated by hypercapnia. These results strongly suggest that AVP V(1A) receptors in the AP may participate in the modulation of cardiopulmonary functions through the activation of V(1A) receptors and the pathway connected to the NTS. They may also indicate that a putative vasopressinergic pathway has a projection to the AP to alter the excitability of neurons having AVP V(1A) receptors and results in an inhibition of cardiopulmonary functions via the connection between the AP and NTS.
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PMID:Vasopressin produces inhibition on phrenic nerve activity and apnea through V(1A) receptors in the area postrema in rats. 1735 38

Copeptin, the C-terminal part of the arginine vasopressin precursor peptide, holds promise as a diagnostic and prognostic plasma biomarker in various acute clinical conditions. Factors influencing copeptin response in the critical care setting are only partially established and have not been investigated systematically. Using an in vivo infant ventilation model (Wistar rats, 14 days old), we studied the influence of commonly occurring stressors in critically ill children. In unstressed ventilated rats basal median copeptin concentration was 22pmol/L. In response to respiratory alkalosis copeptin increased 5-fold, while exposure to hypoxemia, high PEEP, hemorrhage, and psycho-emotional stress produced a more than 10-fold increase. Additionally, we did not find a direct association between copeptin and acidosis, hypercapnia, and hyperthermia. Clinicians working in the acute critical care setting should be aware of factors influencing copeptin plasma concentrations. Moreover, our results do have implications for animal studies in the field of stress research.
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PMID:Determinants of plasma copeptin: a systematic investigation in a pediatric mechanical ventilation model. 2312 68

Mammalian birth is accompanied by a period of obligatory asphyxia, which consists of hypoxia (drop in blood O2 levels) and hypercapnia (elevation of blood CO2 levels). Prolonged, complicated birth can extend the asphyxic period, leading to a pathophysiological situation, and in humans, to the diagnosis of clinical birth asphyxia, the main cause of hypoxic-ischemic encephalopathy (HIE). The neuroendocrine component of birth asphyxia, in particular the increase in circulating levels of arginine vasopressin (AVP), has been extensively studied in humans. Here we show for the first time that normal rat birth is also accompanied by an AVP surge, and that the fetal AVP surge is further enhanced in a model of birth asphyxia, based on exposing 6-day old rat pups to a gas mixture containing 4% O2 and 20% CO2 for 45 min. Instead of AVP, which is highly unstable with a short plasma half-life, we measured the levels of copeptin, the C-terminal part of prepro-AVP that is biochemically much more stable. In our animal model, the bulk of AVP/copeptin release occurred at the beginning of asphyxia (mean 7.8 nM after 15 min of asphyxia), but some release was still ongoing even 90 min after the end of the 45 min experimental asphyxia (mean 1.2 nM). Notably, the highest copeptin levels were measured after hypoxia alone (mean 14.1 nM at 45 min), whereas copeptin levels were low during hypercapnia alone (mean 2.7 nM at 45 min), indicating that the hypoxia component of asphyxia is responsible for the increase in AVP/copeptin release. Alternating the O2 level between 5 and 9% (CO2 at 20%) with 5 min intervals to mimic intermittent asphyxia during prolonged labor resulted in a slower but quantitatively similar rise in copeptin (peak of 8.3 nM at 30 min). Finally, we demonstrate that our rat model satisfies the standard acid-base criteria for birth asphyxia diagnosis, namely a drop in blood pH below 7.0 and the formation of a negative base excess exceeding -11.2 mmol/l. The mechanistic insights from our work validate the use of the present rodent model in preclinical work on birth asphyxia.
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PMID:Surge of Peripheral Arginine Vasopressin in a Rat Model of Birth Asphyxia. 2940 57


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